ライフサイエンスコーパス: nephrosis

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1 se-activated receptor-specific manner during nephrosis.

2 ular damage and podocyte loss induced by PAN nephrosis.

3 ith histopathological findings of congenital nephrosis.

4 response to puromycin aminonucleoside (PAN) nephrosis.

5 function in a rat model of puromycin-induced nephrosis.

6 ween these processes in rats with adriamycin nephrosis.

7 ause of loss of renal function in adriamycin nephrosis.

8 induction of puromycin aminonucleoside (PAN) nephrosis.

9 lointerstitial nephritis associated with PAN nephrosis.

10 uria and how it causes the other findings of nephrosis.

11 pment, abnormal extrapyramidal movements and nephrosis.

12 that transcript levels of the podocyte gene nephrosis 2 homolog (Nphs2), were heritable and controll

13 5.15) for nephritis, nephrotic syndrome, and nephrosis; 4.08 (1.38-12.08) for esophageal cancer; 4.19

14 dence of proteinuria, indicated by relapsing nephrosis after CsA withdrawal, required additional cour

15 Most aging rats display chronic progressive nephrosis, although the rate at which injury develops is

16 Nephrosis and a rapid decline in kidney function charact

17 mbranous nephropathy who exhibited relapsing nephrosis and chronic depression of GFR.

18 in 1 (RIP1) kinase domain, prevented osmotic nephrosis and CIAKI, whereas an inactive Nec-1 derivate

19 linical CIAKI, including RCM-induced osmotic nephrosis and increased serum levels of urea and creatin

20 In the human glomerulopathies minimal-change nephrosis and membranous nephropathy, there is an increa

21 Developments related to the pathogenesis of nephrosis and why some patients develop focal segmental

22 a as a contributor to podocyte injury during nephrosis, and suggest that thrombin and/or podocyte-exp

23 Some patients have nephrosis-associated renal disease characterized by typi

24 ncer, diabetes, nephritis/nephrotic syndrome/nephrosis, chronic lower respiratory disease, and influe

25 he podocytes, leading to the hypothesis that nephrosis develops from an inability to develop a functi

26 n GBM contributes to the renal pathology and nephrosis in NPS.

27 PAN nephrosis increased the protein levels of JAM-A, occludi

28 t the induction of puromycin aminonucleoside nephrosis involves podocyte migration conducted by a coo

29 Puromycin aminonucleoside (PAN)-induced nephrosis is a well-described model of human idiopathic

30 d glomerulopathies, including minimal change nephrosis, membranous glomerulonephritis, and IgA nephro

31 he nephrotic syndrome, the murine adriamycin nephrosis model was used to explore the role of RAGE in

32 rthermore, the rat puromycin aminonucleoside nephrosis model, previously suspected of undergoing SD-T

33 glomerular basement membrane seen in the PAN nephrosis model.

34 with hirudin reduced proteinuria in two rat nephrosis models, and thrombin colocalized with a podocy

35 the candidate region for Finnish congenital nephrosis (NPHS1) in 19q13.1.

36 In puromycin aminonucleoside nephrosis (PAN), GIV expression increased, GIV was phosp

37 nephritis and puromycin aminonucleoside (PA) nephrosis rat models of podocyte injury.

38 d disorder characterized by microcephaly and nephrosis resulting from mutations in the WDR73 gene.

39 y, serologic, and histopathologic indices of nephrosis showed reversal of CG in 8 of 12 CYC202-treate

40 lasma thrombin generation is enhanced during nephrosis, suggesting that thrombin may contribute to ne

41 With nephrosis, there were comparable (greater than twofold)

42 The diagnosis of "osmotic nephrosis" was confirmed by renal biopsy, and the condit

43 Wistar albino rat shows progressive chronic nephrosis with age and therefore was used to determine t

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